My western blot is positive for IgG bands 31 and 34 from Igenex. I have had more than one positive FISH for Babesia microti. I have positive serology for Bartonella henselae and quintana. I have had a positive PCR for Mycoplasma fermentans. All four members of my family, including my somewhat ill but working husband and my clinically healthy son, have similar TBD tests. The only real difference I see in testing, my family and others, is that it is possible that people who respond to antibiotics are more likely to be IgM positive for Lyme specific bands on west blot. My daughter had acute Lyme (with an EM rash and systemic symptoms) that was adequately treated and she was healthy for three years after that. She became ill again in early adolescence without another known tick attachment though we lived in a highly endemic area. My husband had cardiac “Lyme” that did not respond to antibiotics; in fact he developed chronic IBS symptoms due to C. diff from too many antibiotics. He got better just by refusing antibiotics and eating well, but it took a very long time. He still has very significant signs and symptoms of illness, but works at a physically demanding job and is a cyclist. My son who has suspicious Bb tests, was seen by the most well-known Lyme pediatrician in the world who chose not to treat him. There were others in the LLMD community who might have treated him. I shudder to think…
I think the use of antibiotics in this patient population is sometimes necessary but very problematic. There are gut issues already, almost always worsened by the introduction of antibiotics. The way they are being used here is a witch hunt in my opinion. I think that the idea that the progressive neuroimmune disorder seen in the “post Lyme” group is due to cyst forms of Bb is erroneous. Cyst forms exist for many bacterial forms, just as viruses remain unactivated for a lifetime. The patients are sensitive. For many who have been ill for a long time throwing huge doses of antibiotics at it is like shooting at an insect, nasty bug that it may be, with a bazooka. Lots of collateral damage.
It is very difficult for a doctor to tell a patient that there is nothing he or she can do. Patients demand prescriptions. But overprescribing makes things worse. I think you can do what you can to modify the host environment and many will regain a better level of wellness. In my private practice I found that patients often benefited tremendously by helping them to stop many harmful medications. I believe that all drugs are poison. But that doesn’t mean you might not want to take some. It is always a trade off and for many, long term antibiotics have a poor risk benefit ratio. At best it seems that they may postpone the inevitable a bit, but at a great cost.
I DO believe that there is a place for the use of antibiotics in this patient group, though I don’t think that anyone really has a handle on it. My daughter still seems to require some antibiotic coverage, though I believe she is better off if her antibiotics are intermittent. I do better with no antibiotics. It is trial and error for each individual at this point. Unfortunately the error part can be very destructive. In fact, the downside may be as great or greater than the upside. Time will tell for each person. The sad thing is that without clinical trials, all of that experience is wasted for the group as a whole.
It is important to note that the very few doctors who care for both “Lyme” and “ME/CFS” patients are completely unable to distinguish between the conditions clinically. The difference is that the CFS doctors don’t use antibiotics. They are more guilty of the indiscriminate use of antivirals which doesn’t seem from the outside to be as harmful as endless courses and combinations of antibiotics.
My family alone covers the spectrum of disease, but I have a much larger group than that to draw from in forming my opinions. The fact that some people do better with antibiotics doesn’t mean that it is a good idea for everyone who has ever been bitten by a tick. There are LLMDs who will treat on clinical grounds alone, with no supporting serological evidence. I would just like to point out that errors of commission are just as bad as or worse than errors of omission.
I was an ILADS member for six years. I quit recently because I no longer feel an affiliation with it as an organization. That they continue to put forth their “Guidelines” in light of new information is very disappointing, to be polite. I do not think that their ideas are standing up well to the test of time. They seem unable to incorporate new discovery into their thinking and are just continuing to defend their entrenched ideas and past actions. Very sad for patients. It is one thing to be harmed in ignorance, another for physicians to persist in doing what they’ve been doing, even though it doesn’t work, when new information is available. It will all come out in the wash, but many more people will be harmed in the meantime.
I believe that this idea that, even without a clear salutary response, if you only persist long enough with antibiotics you will eventually get well, is a complete myth. The passage of time is not supporting that hypothesis. And believe me, I bought into it, hook, line and big giant sinker, because my daughter responded to antibiotics, until she didn’t. I never did, but that didn’t keep LLMDs from prescribing more and more antibiotics for five years. I have now been off antibiotics for almost a year and I am much better than at any time I was on them. Of course I am penniless from treatment and lost productivity.
Taking a broad spectrum antibiotic knocks down flora in a broad spectrum way. The “herx” is an inflammatory reaction from the release of antigen, but it has little or nothing to do with Bb in my opinion. A Jarisch-Herxheimer reaction is a specific response to treating syphilis and it includes a rash. The “herx” that Lyme patients get is not that, but an indication that the body is not dealing with the die-off. If you knew you had active Bb, you might want to go through it for a little while, but months, years? There must be a proper way to use antibiotics in this patient group, but nobody has a clue at this point. Antibiotics are used all the time with HIV patients to good effect.
I did it. I know many others who have done it. It doesn’t work for most. Find me 10 patients who were sick for years, went on antibiotics, didn’t respond in a few months, kept going anyway and are now “well” years later. In general “chronic Lyme” patients do not get “well”. I presume there is a subset of patients that take antibiotics, get better and go away. But I suspect that anyone who is still searching for the right protocol is unlikely to get well with more antibiotics, in any dose or combination. I presume the people who get well have Bb and that’s it. I know of a few people who have done well on long term (many years) orals and they all had a definite response to treatment. Also they were never were treated with IV’s. They deteriorate quickly if they take a break and have to go back on.
I do not believe that treatment failure is because of co-infections. Bartonella and Babesia are there, but they are cleared or remain dormant in a healthy person. They are opportunists in this patient population. That doesn’t mean that they might not need to be treated sometime. Bartonella henselae is found in endocarditis, but it responds to treatment. The idea that these patients are being treated for suspected Bartonella with nothing more than minimally elevated IgG titers is nuts in my opinion. I know people who have permanent damage form quinolones and aminoglycosides because of the Bartonella witch hunt. Something like 40% of healthy people have positive Bartonella serology. When I lived in the Berkshires I had a darkfield microscope. I didn’t use it diagnostically in my practice. It was a hobby. But I can tell you that Babesia genus is not hard to see. There is even a pathognomonic finding, the Maltese cross, that is very easy to see. I saw live Babesia in the blood of perfectly healthy people in the southern Berkshires (center of Bb epidemic in the US). I am certainly not a microbiologist, but I am old enough to know how to use a microscope.
My own paradigm has shifted. I think that XMRV will turn out to be the underlying cause of all of the neuroimmune illnesses that have become so prevalent over the last 25+ years. My own approach at the moment is to treat my X+ culture with antiretrovirals. But even if I am incorrect, or correct but the drugs don’t work, I think what I am saying about the indiscriminate use of antibiotics is still true. I would use the treatment of other bacterial infections as a guide. If you are on the right tract, expect a response. Even in the treatment of certain infectious diseases that require longer treatment, like TB, leprosy and acne:), the sensible physician expects to see a clear cause and effect for his treatment.
If the causative agent is a retrovirus, the approach to treatment is completely different than that required to treat a bacterial infection. In my opinion, the many metabolic deficits and neuroimmune dysfunction seen in this patient group are much better explained by a viral rather than bacterial etiology. There is a resistance to being labeled with CFS, for good reason, because it is a syndrome without a cure, rather than a disease like Lyme that may be treatable. But treating for the wrong thing will never bring about the desired results.
For me, knowing that the fundamental cause of my illness is a retrovirus changes alternative strategies also. I am at the beginning of the XMRV journey, so my ideas are not yet formulated. However, my private practice was involved with the after effects of brain injury, including Lyme and CFS. The patients I treated with chronic fatiguing illnesses had generally already failed years of antibiotics before they came to me or were intolerant of antibiotics, so I acknowledge a preselected patient population, but I was able to help patients to make progress nevertheless. In particular hormone replacement in physiologic doses can be very useful for both men and women. Also neurofeedback, possibly oxygen therapy and certain herbs may be useful for some people. I also think that there may be a place for cognitive enhancers and “anti-aging” drugs. Carefully discontinuing psychiatric medications in particular, with the support of other therapies, is often very helpful. I think that SSRIs are very problematic in this patient population. They do not address the cause of the depression that is so prevalent, which I believe to be inflammatory in nature. Neurofeedback is very stabilizing and therefore useful for the many neuropsychiatric instabilities seen. There may also be a place for heart rate variability training, a type of biofeedback, for some of the manifestations of dysautonomia. The fundamental premise of complementary and alternative medicine is to support the host environment or tip the balance in favor of wellness. In patients who are very ill and marginally stable, interventions often must be finessed. In my clinic, I saw my patients quite frequently for an hour at a time over a long period of time. That’s what it takes. But even in the most dire of circumstances it is possible to make gains, sometimes even miraculous ones, with very gentle therapies.
The neglect and abuse that the patients have endured and are enduring every day is a complete travesty. But it is not because an efficacious treatment is being withheld. It is interesting that in the CFS community my thoughts have been seen as hopeful, but in the Lyme community no, because of a myth. CFS patients are almost better off because they are not being told that they can be saved by something harmful that is being withheld from them. I am trying to give people new to this problem pause before they dive right in. Taking that first doxycycline was the worst thing I ever did to my body. Antibiotics are not harmless. Lyme treatment took me down completely.
If you feel that something that could make you better is being denied to you, it becomes less important to prove efficacy than to try it. But lots of people have and I believe that there is a great deal of harm being done to patients, some of whom don’t even have active borreliosis, just serology that indicates that the organism is there. Lots of organisms persist in the body without causing active disease at any particular moment. I am not saying that I have the answer to the antibiotic question. It should be possible to consider the question while under the care of a competent infectious disease doctor. But because of the politics of the situation, patients are denied that option. It is a horrible situation, but unfortunately, endless antibiotics will not fix it. When people are very invested in a treatment, it is almost impossible for them to sort out what is going on. That goes for doctors and patients. I wish I could say, find a smart ID doctor to work with. But we all know that there are almost no competent doctors interested in treating this disease. So as a patient group we are on our own. My best advice is to find a compassionate GP to work with. And always remember that sometimes it is better to do nothing until a clear course of action presents itself. Primum non nocere.
False hope never helped anyone. Personally, I am hopeful that we will soon have an approach to this illness that is based on more than hoping.
Below are links to a few papers on measurement and modeling of the decay characteristics of HIV with treatment. It is worth noting that there is a first-phase rapid decay and a much slower second-phase decay. Though the exact mechanism for the later is still unknown, it is likely related to the infection of long-lived cells. Second-phase decay in AIDS patients treated with HAART takes years.
Raltegravir alters decay kinetics of HIV
Decay dynamics of HIV-1
Dendritic cells and decay of HIV
Personally, I feel best about AZT right now of the three drugs available. It prevents replication at the most basic point in the virus’ life cycle. It is the broadest spectrum if you will. It has been around the longest. There is vast experience with it over many years of treatment. It may be that raltegravir requires reduction of viral load before adding. Or it may be that we are like the genetically susceptible infected mice for whom it isn’t the right drug (Raltegravir autoimmunity). We desperately need viral load measures and organized clinical trials. But until then, I’ll keep reporting…
I have heard from people considering AZT alone, sometimes at below HIV doses. I would still prefer more than one drug. We can’t know anything about how readily this virus will become resistant to drugs. We don’t know anything about XMRV’s RT error rate. We don’t know anything about viral load in target tissues.
I stayed off both drugs, on AZT alone, for 5 days. I continued to get sicker until I was well below baseline. Last night it seemed clear to me that I had been better off on the AZT/raltegravir protocol, so I decided to go back on raltegravir. Amazingly, I feel much better today. The horribleness seems to be fading into the background again. I am reporting now because I don’t know how it is going to turn out. But it is an almost A-B-A experiment. However the experiment turns out, what has happened already greatly surprises me.
It would have been a fairy tale if the drugs had just worked. So much for logic! I actually didn’t expect it to be that easy. The good news is that if the drugs can move the illness, it is supportive of the hypothesis that XMRV is causative in the pathogenesis of the disease. It seems to me, that if altering the viral load, or altering the build-up of viral particles in the cytoplasm can shift the clinical picture in either direction in days or weeks, viral replication must not be so slow. It is a pretty stunning observation if you think about it. Must be a really good (successful) pathogen to be replicating so freely in relative equilibrium with the host over so many years. Doesn’t kill for a very long time. Clinical observation is that trying to alter things often doesn’t work out so well with CFS patients. Hence the observation that the patients are “sensitive”. Actually I think we are very tough.
When I first saw the Science paper a few days after it was published, it was an ah-ha experience for me. I knew very little about viruses and almost nothing about retroviruses. But what little I did know enabled a fusion of everything I’d learned as a doctor and a patient. So much so, that as I sent my daughter’s and my blood for culture, I thought, if it isn’t this one, there’s another one out there. Here was the fundamental cause of all the subtle and not so subtle things that had gone wrong with my entire family, including the opportunistic infections, the genetic piece, an explanation for vertical transmission and even the activation by stress that matched my direct experience (the virus has a glucocorticoid receptor element in it’s promotor region). I also saw X in my family of origin, members of whom have had aggressive prostate cancer, autistic spectrum disorder and Lyme Disease. So I had a lot of clues.
I am an ER doctor by nature still. Triage. Impact the process where you can. Take care of the people circling the drain first. I am very far down the road so I am in that category.